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Journal of
M e d i cal &
Allied Sciences
Free radicals, oxidative stress and importance of
antioxidants in human health
Amit Kunwar and K.I. Priyadarsini
Radiation and Photochemistry Division,
Bhabha Atomic Research Centre, Trombay, Mumbai-400085, India.
Article history: Abstract
Received 13 March 2011
Revised 04 May 2011
Accepted 14 June 2011
Early online 01 July 2011
Print 31 July 2011
Corresponding author
Amit Kunwar
Radiation and Photochemistry Division,
Bhabha Atomic Research Centre,
Mumbai-400085, India.
Phone: +91 22 25595399
Fax: +91 22 25505151
Email: kamit@barc.gov.in
eactive oxygen species (ROS) is a collective
term used for a group of oxidants, which are
either free radicals or molecular species capable
of generating free radicals. Intracellular generation
of ROS mainly comprises superoxide (O2 − )
radicals and nitric oxide (NO ) radicals. Under normal
physiologic conditions, nearly 2% of the oxygen
consumed by the body is converted into O2 −
through mitochondrial respiration, phagocytosis,
etc 1 . ROS percentage increases during infections,
exercise, exposure to pollutants, UV light, ionizing
radiation, etc. NO , is an endothelial relaxing factor
and neurotransmitter, produced through nitric oxide
synthase enzymes. NO and O2 − R
radicals, are converted
to powerful oxidizing radicals like hydroxyl
Reactive oxygen species (ROS) is a collective term used for oxygen
containing free radicals, depending on their reactivity and oxidizing
ability. ROS participate in a variety of chemical reactions with biomolecules
leading to a pathological condition known as oxidative
stress. Antioxidants are employed to protect biomolecules from the
damaging effects of such ROS. In the beginning, antioxidant research
was mainly aimed at understanding free radical reactions of
ROS with antioxidants employing biochemical assays and kinetic
methods. Later on, studies began to be directed to monitor the ability
of anti-oxidants to modulate cellular signaling proteins like receptors,
secondary messengers, transcription factors, etc. Of late several
studies have indicated that antioxidants can also have deleterious
effects on human health depending on dosage and bioavailability.
It is therefore, necessary to validate the utility of antioxidants
in improvement of human health in order to take full advantage
of their therapeutic potential.
Key words: Reactive oxygen species, oxidative stress, antioxidant
supplementation
© 2011 Deccan College of Medical Sciences. All rights reserved.
radical ( OH), alkoxy radicals (RO ), peroxyl radicals
(ROO ), singlet oxygen ( 1 O2) by complex transformation
reactions. Some of the radical species are
converted to molecular oxidants like hydrogen peroxide
(H2O2), peroxynitrite (ONOO ), hypochlorous
acid (HOCl). Sometimes these molecular species
act as source of ROS.
For example, H2O2 is converted to OH radicals by
Fenton reaction and HOCl through its reaction with
H2O2 can be converted to 1 O2. ONOO at physiological
concentrations of carbon dioxide becomes a
source of carbonate radical anion (CO3 ) 1 . The various
pathways involved in the generation of ROS are
given in fig 1.
53

Kunwar A et al. Free radicals, oxidative stress and antioxidants in human health
ROS in normal physiology
Typically, low concentration of ROS is essential for
normal physiological functions like gene expression,
cellular growth and defense against infection. Sometimes
they also act as the stimulating agents for biochemical
processes within the cell 2 . ROS exert their
effects through the reversible oxidation of active
sites in transcription factors such as nuclear factorkappa
B (NF-kB) and activator protein-1 (AP-1) leading
to gene expression and cell growth 3 . ROS can
also cause indirect induction of transcription factors
by activating signal transduction pathways 3 . One
example of signal transduction molecules activated
by ROS is the mitogen activated protein kinases
(MAPKs). ROS also appear to serve as secondary
messengers in many developmental stages. For
example, in sea urchins ROS levels are elevated
during fertilization. Similarly prenatal and embryonic
development in mammals has also been suggested
to be regulated by ROS 3 . Apart from these; ROS
also participate in the biosynthesis of molecules
such as thyroxin, prostaglandin that accelerate developmental
processes. It is noteworthy that in thyroid
cells, regulation of H2O2 concentration is critical
for thyroxine synthesis, as it is needed to catalyze
the binding of iodine atoms to thyroglobulin 3 . Finally
ROS are also used by the immune system. For example,
ROS have been shown to trigger proliferation
of T cells through NF-кB activation. Macrophages
and neutrophils generate ROS in order to kill the
bacteria that they engulf by phagocytosis. Furthermore,
tumor necrosis factor (TNF-α) mediates the
cytotoxicity of tumor and virus infected cells through
ROS generation and induction of apoptosis 2,3 .
Fig 1. Production of free radicals via different routes
ROS induced oxidative damages
Depending upon their nature, ROS (for e.g. OH radicals)
reactions with biomolecules such as lipid, protein
and DNA, produce different types of secondary
radicals like lipid radicals, sugar and base derived
radicals, amino acid radicals and thiyl radicals.
These radicals in presence of oxygen are converted
to peroxyl radicals. Peroxyl radicals are critical in
biosystems, as they often induce chain reactions 1 .
The biological implications of such reactions depends
on several factors like site of generation, nature
of the substrate, activation of repair mechanisms,
redox status among many others 4 .
For example, cellular membranes are vulnerable to
the oxidation by ROS due to the presence of high
concentration of unsaturated fatty acids in their lipid
components. ROS reactions with membrane lipids
cause lipid peroxidation, resulting in formation of
lipid hydroperoxide (LOOH) which can further decompose
to an aldehyde such as malonaldehyde, 4hydroxy
nonenal (4-HNE) or form cyclic endoperoxide,
isoprotans, and hydrocarbons. The consequences
of lipid peroxidation are cross linking of
membrane proteins, change in membrane fluidity
and formation of lipid-protein, lipid-DNA adduct
which may be detrimental to the functioning of the
cell 5 .
Proteins can undergo direct and indirect damage
following interaction with ROS resulting in to peroxidation,
changes in their tertiary structure, proteolytic
degradation, protein-protein cross linkages and
fragmentation 5 . The side chains of all amino acid
residues of proteins, in particular tryptophan, cyste-
J Med Allied Sci 2011; 1(2) 54

Kunwar A et al. Free radicals, oxidative stress and antioxidants in human health
ine and methionine residues are susceptible to oxidation
by ROS. Protein oxidation products are usually
carbonyls such as aldehydes and ketones.
Although DNA is a stable, well-protected molecule,
ROS can interact with it and cause several types of
damage such as modification of DNA bases, single
and double strand DNA breaks, loss of purines (apurinic
sites), damage to the deoxyribose sugar, DNAprotein
cross-linkage and damage to the DNA repair
system 5 . Not all ROS can cause DNA damage and
OH radical is one of the potential inducers of DNA
damage. A variety of adducts are formed on reaction
of OH radical with DNA. The OH radical can attack
purine and pyrimidine bases to form OH radical adducts,
which are both oxidizing and reducing in nature.
This induces base modifications and sometimes
release of bases. Some of the important base
modifications include 8-hydroxydeoxyguanosine (8-
OHdG), 8 (or 4-, 5-)-hydroxyadenine, thymine peroxide,
thymine glycols and 5-(hydroxymethyl) uracyl 5 .
Free radicals can also attack the sugar moiety,
which can produce sugar peroxyl radicals and subsequently
inducing strand brakeage. The consequence
of DNA damage is the modification of genetic
material resulting in to cell death, mutagenesis,
carcinogenesis and ageing.
Antioxidants and natural defense from ROS induced
damages
Uncontrolled generation of ROS can lead to their
accumulation causing oxidative stress in the cells.
Therefore, cells have evolved defense mechanisms
for protection against ROS mediated oxidative damage.
These include antioxidant defenses to keep a
check on the generation of ROS. An antioxidant is a
substance that is present at low concentrations and
significantly delays or prevents oxidation of the oxidizable
substrate 6 . Antioxidants are effective because
they can donate their own electrons to ROS
and thereby neutralizing the adverse effects of the
latter. In general, an antioxidant in the body may
work at three different levels: (a) prevention - keeping
formation of reactive species to a minimum e.g.
desferrioxamine (b) interception - scavenging reactive
species either by using catalytic and noncatalytic
molecules e.g. ascorbic acid, alphatocopherol
and (c) repair - repairing damaged target
molecules e.g. glutathione 6 . The antioxidant systems
are classified into two major groups, enzymatic antioxidants
and non enzymatic antioxidants. Enzymatic
antioxidants present in the body include superoxide
dismutase (SOD), catalase and glutathione peroxidase
(GPx) that act as body’s first line of defense
against ROS by catalyzing their conversion to less
reactive or inert species (Fig 2) 7 .
J Med Allied Sci 2011; 1(2)
Fig 2. Removal of different reactive oxygen species by antioxidant
enzymes
Several low molecular weight molecules present
inside the cell provide secondary defense against
free radicals. A few examples of such molecules
include glutathione (GSH), α-tocopherol, ascorbate,
bilirubin, etc 6 . These agents either scavenge the
ROS directly or prevent the production of ROS
through sequestration of redox active metals like
iron and copper.
Redox state and oxidative stress
All forms of life maintain a steady state concentration
of ROS determined by the balance between
their rates of production and their rates of removal
by various antioxidants. Thus each cell is characterized
by a particular concentration of reducing species
like GSH, NADH, FADH, etc. stored in many
cellular constituents which determines the redox
state of a cell 6 . By definition redox state is the total
reduction potential or the reducing capacity of all the
redox couples such as GSSG/2GSH, NAD+/NADH,
Asc •− /AcsH − , etc found in biological fluids, organelles,
cells or tissues 8 . Redox state not only describes
the state of a redox pair, but also the redox
environment of a cell. Under normal conditions, the
redox state of a biological system is maintained towards
more negative redox potential values. However,
with increase in ROS generation or decrease
in antioxidant protection within cells, it is shifted towards
less negative values resulting in the oxidizing
environment (Fig 3). This shift from reducing status
to oxidizing status is referred as oxidative stress 6,8 .
During elevated oxidative stress, there is loss of mitochondrial
functions, which results in to ATP depletion
and necrotic cell death, while moderate oxidation
can trigger apoptosis. There are a few recent
reports have shown evidence that the induction of
apoptosis or necrosis during oxidative stress is actually
determined by the redox state of cell 8 . For example
it has been reported that an increase in reduction
potential of +72 mV in HL-60 cells (i.e., from
-239 ± 6 to -167 ± 9 mV) or an increase of +65 mV
in murine hybridoma cells (i.e., from -235 ± 5 to -170
55

Kunwar A et al. Free radicals, oxidative stress and antioxidants in human health
± 8 mV) would cause induction of apoptosis 8 . Oxidative
stress has been implicated in a number of human
diseases like cancer, atherosclerosis, diabetics,
neurological diseases such as Alzheimer's disease,
Parkinson's disease, etc. as well as in the ageing
process.
Fig 3. Balance between oxidant and antioxidant defines oxidative
stress
Antioxidant supplementation
Although cells are equipped with an impressive repertoire
of antioxidant enzymes as well as small antioxidant
molecules, these agents may not be sufficient
enough to normalize the redox status during
oxidative stress 9 . Under such conditions supplementation
with exogenous antioxidants is required to
restore the redox homeostasis in cells. Recent epidemiological
studies have shown an inverse correlation
between the levels of established antioxidants
(vitamin E and C) / phytonutrients present in tissue /
blood samples and cardiovascular disease, cancer
and with mortality due to these diseases 10-12 . Since
several plant products are rich in antioxidants and
micronutrients, it is likely that dietary antioxidant
supplementation protects against the oxidative
stress mediated disease development. Therefore, to
maintain optimal body function, antioxidant supplementation
has become an increasingly popular practice.
Researchers are now attempting to develop
new antioxidants either of natural or synthetic origin.
Natural products as antioxidants
A variety of dietary plants including grams, legumes,
fruits, vegetables, tea, wine etc. contain antioxidants.
The prophylactic properties of dietary plants
have been attributed to the antioxidants / polyphenols
present in them. Polyphenols with over 8000
structural variants are secondary metabolites of
J Med Allied Sci 2011; 1(2)
plants and represent a huge gamut of substances
having aromatic ring(s) bearing one or more hydroxyl
moieties 13 . Polyphenols are effective ROS scavengers
and metal chelators due to the presence of
multiple hydroxyl groups. Examples of polyphenolic
natural antioxidants derived from plant sources include
vitamin E, flavonoids, cinnamic acid derivatives,
curcumin, caffeine, catechins, gallic acid derivatives,
salicylic acid derivatives, chlorogenic acid,
resveratrol, folate, anthocyanins and tannins 13 . Apart
from polyphenols there are also some plant derived
non-phenolic secondary metabolites such as melatonin,
carotenoids, retinal, thiols, jasmonic acid, eicosapentaenoic
acid, ascopyrones and allicin that
show excellent antioxidant activity 14,15 . Vitamin C,
the water soluble natural vitamin, plays a crucial role
in regenerating lipid soluble antioxidants like vitamin
E 6 . Both vitamin E and C are used as standards for
evaluating the antioxidant capacity of new molecules
6 . As an example, the antioxidant activity of
curcumin has been discussed in some detail in the
following section.
Curcumin a well-known natural antioxidant
Curcumin is a yellow pigment, the major constituent
of turmeric. It is a diferuloyl methane having an unsaturated
-diketone, and phenolic groups. It exhibits
a variety of pharmacological properties such as
anti-inflammatory, anti-carcinogenic, anti-microbial,
neuro-protective,cardio-protective,thrombo suppressive
and anti-diabetic actions 16,17 . The compound is
considered as a potent anti-cancer agent and is currently
being evaluated in different stages of clinical
trials against a variety of cancers 16 .
Curcumin is also a potent antioxidant. Studies from
our laboratory as well as others have shown it to be
an excellent scavenger of ROS such as O2 − radicals,
lipid peroxyl radicals, OH radicals and nitrogen
dioxide radicals, whose production is implicated in
the induction of oxidative stress 18,19 . Its free radical
scavenging ability is comparable to well known antioxidants
like vitamins C and E 19 . It has been shown
to inhibit lipid peroxidation in a variety of in vitro
models such as rat brain homogenates, rat liver microsomes,
erythrocytes, liposomes, and macrophages,
where peroxidation is induced by Fenton
reagent, H2O2, radiation and 2,2-azo-bis(2amidinopropane)
hydrochloride (AAPH) 19 . It has also
been reported to inhibit singlet oxygen-stimulated
DNA cleavage in plasmid pBR322 DNA, H2O2 and
AAPH induced hemolysis of erythrocytes 19,20 . In epithelial
cells, curcumin has been shown to increase
GSH levels which, in turn lead to lowered ROS production
21 . It also mediates its antioxidative effects by
elevating the levels of phase II enzymes such as
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Kunwar A et al. Free radicals, oxidative stress and antioxidants in human health
NAD(P)H:quinone reductase (QR) and antioxidant
enzymes like SOD, GPx and hemeoxygenase
(HO) 21,22 . For example, our previous study have
found that curcumin induces the expression of SOD,
GPx and HO-1 in RAW 264.7 (murine macrophage)
cells contributing to its antioxidant effects 22 . Similarly,
the in vitro incubation of bovine aortic endothelial
cells and human proximal renal tubular cells with
curcumin has been reported to result in dose and
time dependent increase of HO-1 mRNA, protein
expression and enzymatic activity 23 . The postulated
mechanism for these actions involves the activation
of PKC pathways and antioxidant response element
(ARE) mediated transcriptional induction. Curcumin
has also been shown to inhibit oxidative damage in
different animal models. For example, it inhibited
lipid degradation and decreased ischemia-induced
biochemical changes in heart in the feline model. In
a focal cerebral ischemia model of rats, it offered
significant neuroprotection through inhibition of lipid
peroxidation, increase in endogenous antioxidant
defense enzymes and reduction in peroxynitrite formation
24 . Further, studies on the mechanistic aspects
of antioxidant activity revealed that phenolic
hydroxyl groups of curcumin play a significant role in
its diverse antioxidant activity 25 . Some reports suggested
that both hydroxyl and diketone groups exert
antioxidant properties. The phenolic hydroxyl groups
give ROS scavenging ability and the diketone structure
is considered to be responsible for its ability to
bind to metals. The ability of curcumin to act as an
antioxidant in the presence of metals arises mainly
by preventing the Fenton chemistry within cells
through chelation of free metal ions such as Cu +2 ,
Fe +2 , etc 26 . There are some reports which indicate
that stable metal complexes of curcumin exhibit
higher antioxidant activity as compared to native
curcumin molecule. The manganese complexes of
curcumin were found to show greater SOD activity,
hydroxyl radical scavenging activity, and nitric oxide
radical scavenging activity than the parent molecules
27 . Similarly, our group has reported that copper
complex of curcumin also exhibits antioxidant,
superoxide-scavenging and SOD enzyme mimicking
activities superior to those of curcumin itself 28 .
These copper curcumin complexes were found better
than curcumin in preventing the γ-radiation induced
oxidative stress in splenic lymphocytes. The
associated mechanisms responsible for above effects
were identified as activation of cytoprotective
signaling components like protein kinase C delta
(PKC) and nuclear factor-B (NF--B) in temporally
relevant manner 29 . Thus, curcumin exhibits a variety
of antioxidant effects and appears to have a significant
potential in the treatment of multiple diseases
that are mediated through oxidative stress.
J Med Allied Sci 2011; 1(2)
Interestingly, reports are now appearing about apparently
contradictory pro-oxidative effects of curcumin.
For example, curcumin induced DNA fragmentation
and base damage in the presence of copper
and isozymes of cytochrome p450 (CYP) that
are present in lung, lymph, liver, and skin 30 . The authors
hypothesized that the damage was the result
of CYP-catalyzed O-demethylation of curcumin,
leading to the formation of an O-demethyl curcumin
radical, which, in the presence of copper, formed a
DNA-damaging Cu(I)-hydroperoxo complex. DNA
damage was attenuated when concentrations of
curcumin exceeded those of copper, presumably
due to the chelation of copper by curcumin. Copper
dependent formation of 8-hydroxy-deoxyguanosine
in response to curcumin was also reported (Yoshino
et al., 2004) and linked to apoptotic cell death in
HL60 cells 31 . Similarly, curcumin-mediated DNA
damage was also reported in mouse lymphocytes. In
agreement with these reports we also observed that
although curcumin inhibited that AAPH induced lipid
peroxidation and hemolysis in erythrocytes, it could
not prevent the leakage of K + ions. Rather, curcumin
itself induced K + ion release and GSH depletion at
higher concentration suggesting its pro-oxidant nature
20 . Further, our group has reported that curcumin
induced the ROS generation and GSH depletion in
RAW 264.7 cells in a concentration and time dependant
manner 22 . Of late, several reports have
emerged demonstrating pro-oxidative nature of curcumin,
in view of its ability to promote oxidative
stress in transformed cells in culture. These effects
have been correlated with enhanced ROS production,
alteration of the cellular redox homeostasis
(e.g., the depletion of glutathione), and disruption of
the mitochondrial functions e.g., dissipation of mitochondrial
inner transmembrane potential 32-35 . The
enhancement of oxidative stress by curcumin in
transformed cells ultimately results in mitochondrialmediated
apoptosis, and this has been considered
as one of the mechanisms responsible for the anticancer
activity of curcumin 32-35 . The mechanism by
which curcumin mediates its pro-oxidant effects is
not completely understood. However, some reports
suggest that curcumin irreversibly binds to mitochondrial
thioredoxin reductase, and modifies its
activity in to NADPH oxidase through alkylation of
cysteine residue present in the catalytically active
site of the enzyme 35 . This leads to the production of
ROS, which according to few others is due to the
α,β-unsaturated carbonyl moiety of curcumin 19 . The
pro-oxidant property is also believed to be due to the
generation of phenoxyl radicals of curcumin by
heme peroxidase-H2O2 system. These phenoxyl
radicals could be repaired by cellular GSH or NADH.
In this process, the resulting GS radical forms
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Kunwar A et al. Free radicals, oxidative stress and antioxidants in human health
GSSG radical and this may further reduce O2 to
form O2 radical leading to elevated ROS levels 36 .
In short, all these published reports support that curcumin
may switch from antioxidant to pro-oxidant
depending on cell type, redox environment and dosage.
A few reports also suggest that curcumin acts
as an antioxidant in normal cells while showing preferable
pro-oxidant behavior in tumor cells. It is this
differential property of curcumin, which makes it a
potent anti-tumor agent. The chemical structure of
curcumin and its reported antioxidant and prooxidant
mechanisms has been shown in fig 4.
Synthetic compounds as antioxidants
The use of synthetic compounds possessing antioxidant
activity for the preservation of cosmetic,
pharmaceutical and food products has been a common
practice. The most commonly used synthetic
antioxidants in the food industry are butylated 4hydroxytoluene
(BHT) and butylated 4hydroxyanisole
(BHA) 37 . However, the use of synthetic
antioxidants in the health industry has been
fraught with concerns about the toxicity associated
with synthetic compounds 16 . There are numerous
reports indicating that polyphenols which are the
major constituent of most of the natural antioxidants
are poorly bio-absorbed and the concentrations
achieved in the target tissues are sub-therapeutic in
vitro 38 . These findings have shifted the attention of
researches towards the development of synthetic,
water soluble, stable and nontoxic compounds with
potent antioxidant activity and therapeutic application.
Many different antioxidants and antioxidant
compositions have been developed over the years
based on their mechanism of action.
One group of such antioxidants includes molecules
that prevent the production of ROS through metal
ions sequestration, free radical scavenging or by
inhibiting the ROS producing enzymes. For example,
desferrioxamine an iron chelator have been
tested for preventing ROS formation in a myocardial
stunning model system following hemorrhagic and
endotoxic shock 39 . The allopurinol and other pyrazolopyrimidines,
which are inhibitors of xanthine oxidase,
have also been tested under similar disease
model system and have been found to be very effective.
Several congeners of GSH have been used in
various animal models to attenuate ROS induced
injury. For example, N-2-mercaptopropionylglycine
has been found to confer protective effects in a canine
model of myocardial ischemia and reperfusion
and N-acetylcysteine (NAC) has been used to treat
endotoxin toxicity in sheep. Dimethyl thiourea
(DMTU) and butyl-phenylnitrone (BPN) are believed
to scavenge hydroxyl radical, and have been shown
J Med Allied Sci 2011; 1(2)
to reduce ischemia reperfusion injury in rat myocardium
and in rabbits 40 .
Another important group of synthetic antioxidants
includes molecules that act as antioxidant enzyme
mimic and catalytically remove the ROS. For example,
the complex formed between the chelator, desferroxamine
and manganese possesses SOD activity
and has shown some activity in biological models,
but the instability of the metal ligand complex apparently
precludes its pharmaceutical use. Porphyrinmanganese
and curcumin-transition metal complexes
have also shown SOD activity and are under development
as SOD mimetic drugs 27 . Ebselen an organoselenium
compound exhibits GPx activity and
has been tested in clinic as anti-inflammatory drug 41 .
Recently our group has also been engaged in the
development of aliphatic water-soluble selenium
compounds as antioxidants. One such compound
diseledipropionic acid showed significant antioxidant
activity and potent in vivo radioprotection against
exposure to lethal dose of γ-radiation 42 .
Based on these studies, it is clear that a need exists
for antioxidant agents, which are efficient in removing
ROS, inexpensive to manufacture, stable, and
possess advantageous pharmacokinetic properties,
such as the ability to cross the blood-brain barrier
and penetrate tissues. Such versatile antioxidants
would find use as pharmaceuticals and possibly as
neutraceuticals.
Limitations of antioxidant supplementation
The primary concern regarding antioxidant supplementation
is their potentially deleterious effects on
ROS production (pro-oxidant action) especially when
precise modulation of ROS levels are needed to allow
normal cell function 43 . In fact, some negative
effects of antioxidants when used in dietary supplements
(flavanoids, carotenoids, vitamin C and synthetic
compounds) have emerged in the last few
decades 11,12,44 . Mechanistic investigation has revealed
that antioxidants may exhibit pro-oxidant activity
depending on the specific set of conditions. Of
particular importance are their dosage, redox conditions
and also the presence of free transition metals
in cellular milieu 36,44 . For example, ascorbate, a wellknown
antioxidant in the presence of high concentration
of ferric iron is a potent mediator of lipid peroxidation.
Recent studies suggest that ascorbate
sometimes increases DNA damage in humans. Similarly
β-carotene also can behave as a pro-oxidant
in the lungs of smokers. Of note, natural antioxidant
compounds have relatively poor bioavailability. It is
therefore necessary to take into cognizance the bioavailability
and differential activities of natural and
synthetic antioxidant compounds before considering
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Kunwar A et al. Free radicals, oxidative stress and antioxidants in human health
J Med Allied Sci 2011; 1(2)
Fig 4. Important factors controlling the antioxidant and pro-oxidant activities of curcumin
them as therapeutic or pharmacological agents.
Conclusion
In this regard it is worth mentioning that at present
several natural as well as synthetic compounds are
available in the market as antioxidant supplements
in different formulations like capsules, tablets, etc.
with a direction to be consumed under specific diseased
condition. However, as a caution it is advised
to undertake the consumption of such supplements
only under a strict medical supervision in order to
avoid the dosage related negative effects.
Acknowledgments
The authors are also grateful to Dr. S.K. Sarkar,
Head, RPC Division and Dr. T. Mukherjee, Director,
Chemistry Group, BARC for encouragement.
Conflict of interest: None
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